Zinc is the authoritative metal which is present in our body, and reactive zinc metal is crucial for neuronal signaling and is largely distributed within presynaptic vesicles. Zinc also plays an important role in synaptic function. At cellular level, zinc is a modulator of synaptic activity and neuronal plasticity in both development and adulthood. Different importers and transporters are involved in zinc homeostasis. ZnT-3 is a main transporter involved in zinc homeostasis in the brain. It has been found that alterations in brain zinc status have been implicated in a wide range of neurological disorders including impaired brain development and many neurodegenerative disorders such as Alzheimer's disease, and mood disorders including depression, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and prion disease. Furthermore, zinc has also been implicated in neuronal damage associated with traumatic brain injury, stroke, and seizure. Understanding the mechanisms that control brain zinc homeostasis is thus critical to the development of preventive and treatment strategies for these and other neurological disorders.

Immunoinformatics plays a pivotal role in vaccine design, immunodiagnostic development, and antibody production. In the past, antibody design and vaccine development depended exclusively on immunological experiments which are relatively expensive and time-consuming. However, recent advances in the field of immunological bioinformatics have provided feasible tools which can be used to lessen the time and cost required for vaccine and antibody development. This approach allows the selection of immunogenic regions from the pathogen genomes. The ideal regions could be developed as potential vaccine candidates to trigger protective immune responses in the hosts. At present, epitope-based vaccines are attractive concepts which have been successfully trailed to develop vaccines which target rapidly mutating pathogens. In this article, we provide an overview of the current progress of immunoinformatics and their applications in the vaccine design, immune system modeling and therapeutics.

The present work deals with the development of pectin-gelatin (PEGE) hydrogel membranes for wound dressing applications. The prepared hydrogels were characterized by FTIR spectroscopy, XRD spectroscopy, water vapor transmission rate (WVTR) test and tensile strength test. Morphology and thermal stability of the membranes were analyzed by Field emission scanning electron microscopy (FESEM) and thermogravimetric analysis (TGA). The swelling studies of the hydrogels were conducted in different pH buffer solutions (pH 1.4, 5.4, 7.4 and 9.4). FTIR spectra of the hydrogels indicated considerable lowering in usual -OH stretching vibration peak of pectin and gelatin, which suggests the development of probable intermolecular interactions between the two natural polymers. XRD study revealed the decrease in crystallinity of hydrogels as compared to parent pectin. The morphological analysis of the hydrogel revealed highly interconnected honeycomb type architecture with pore size ranging from 10 to 40 μm. It was found that increase in gelatin ratio significantly improves the porous nature of the membranes. TGA study showed the enhanced thermal stability of PEGE hydrogel as compared to reference pectin. Tensile strength (TS) and elongation at break (EB) was found to increase with gelatin content in the hydrogel membranes but further increase leads to decrease in TS and EB. The WVTR analysis of the membranes showed the moisture Int J Plast Technol (June 2011) 15(1):82-95 retentive properties indicating its possible use in moist wound care. The PEGE hydrogels were found to be cytocompatible with B16 melanoma cells.

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Nutritional interventions are now recommended as strategies to delay Alzheimer's disease (AD) progression. The present study evaluated the neuroprotective effect (anti-inflammation) of lactic acid bacteria (either Lactobacillus fermentum LAB9 or L. casei LABPC) fermented cow's milk (CM) against lipopolysaccharide (LPS)-activated microglial BV2 cells in vitro. The ability of CM-LAB in attenuating memory deficit in LPS-induced mice was also investigated. ICR mice were orally administered with CM-LAB for 28 d before induction of neuroinflammation by LPS. Learning and memory behaviour were assessed using the Morris Water Maze Test. Brain tissues were homogenised for measurement of acetylcholinesterase (AChE), antioxidative, lipid peroxidation (malondialdehyde (MDA)) and nitrosative stress (NO) parameters. Serum was collected for cytokine analysis. CM-LAB9 and CM-LABPC significantly (P < 0·05) decreased NO level but did not affect CD40 expression in vitro. CM-LAB attenuated LPS-induced memory deficit in mice. This was accompanied by significant (P < 0·05) increment of antioxidants (SOD, GSH, GPx) and reduction of MDA, AChE and also pro-inflammatory cytokines. Unfermented cow's milk (UCM) yielded greater cytokine lowering effect than CM-LAB. The present findings suggest that attenuation of LPS-induced neuroinflamation and memory deficit by CM-LAB could be mediated via anti-inflammation through inhibition of AChE and antioxidative activities.